Bacterial pathogens of plant and animals use the type III secretion (T3S) system and effector protein substrates to alter eukaryotic physiology to promote bacterial multiplication and host colonization. The large repertoire of T3S effectors (~20-30 proteins) in plant pathogenic bacteria predicts that multiple nodes in plant signaling cascades are being targeted. The identity of the plant targets and the biochemical mechanisms by which these T3S effector proteins manipulate plant physiology however are poorly understood. Extensive phenotypic studies support the concept that many of the T3S effectors suppress the plant immune system to colonize tissues. This illuminates the importance of basal defense responses and resistance (R) protein-mediated innate immune responses in controlling the outcome of bacterial infections in the plant kingdom. Understanding how plant immunity is regulated and how bacterial pathogens manipulate their hosts is fundamental knowledge required for the prevention and elimination of plant disease. The long-term goal of this project is elucidate how plants integrate lipid signals to respond to bacterial infection. Two conserved eukaryotic proteins - SOBER1, a lipase and CIP, a putative apolipoprotein - have been identified and shown to be important regulators of innate immune responses in plants. Comprehensive genetic and biochemical studies will be performed using the Arabidopsis pathosystem to characterize SOBER1 and CIP substrate specificity and to determine the mechanisms by which these proteins control phospholipid metabolism and signaling during bacterial infection. Studies will also be aimed to determine the biochemical mechanisms by which the pathogen T3S effector AvrBsT perturbs lipid homeostasis within infected plant cells. This work is expected to provide fundamental insight to the biochemical mechanisms used by plants to control lipid metabolism and signaling in response to pathogen attack. The growing body of evidence suggesting an interplay between lipid metabolism and immunity in both plants and animals indicates that fundamental knowledge about how lipid signals are initiated and terminated will be essential to fully understand how the immune system is regulated in eukaryotes.